| + |
F11 | up-regulates activity 
cleavage
|
HGF |
0.317 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256515 |
Arg424 |
KNMEDLHrHIFWEPD |
in vitro |
|
| pmid |
sentence |
| 12372819 |
the ability of plasma kallikrein and FXIa to activate pro-HGF in vitro raises the possibility that mediators of inflammation and blood coagulation may also regulate processes that involve the HGF/c-Met pathway, such as tissue repair and angiogenesis.Unlike other known activators, both FXIa and kallikrein processed pro-HGF by cleavage at two sites. Using N-terminal sequencing they were identified as the normal cleavage site Arg(494)-Val(495) and the novel site Arg(424)-His(425) located in the K4 domain of the alpha-chain. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256514 |
Arg494 |
CAKTKQLrVVNGIPT |
in vitro |
|
| pmid |
sentence |
| 12372819 |
the ability of plasma kallikrein and FXIa to activate pro-HGF in vitro raises the possibility that mediators of inflammation and blood coagulation may also regulate processes that involve the HGF/c-Met pathway, such as tissue repair and angiogenesis.Unlike other known activators, both FXIa and kallikrein processed pro-HGF by cleavage at two sites. Using N-terminal sequencing they were identified as the normal cleavage site Arg(494)-Val(495) and the novel site Arg(424)-His(425) located in the K4 domain of the alpha-chain. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
KLKB1 | up-regulates activity
cleavage
|
HGF |
0.328 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256513 |
Arg424 |
KNMEDLHrHIFWEPD |
in vitro |
|
| pmid |
sentence |
| 12372819 |
the ability of plasma kallikrein and FXIa to activate pro-HGF in vitro raises the possibility that mediators of inflammation and blood coagulation may also regulate processes that involve the HGF/c-Met pathway, such as tissue repair and angiogenesis.Unlike other known activators, both FXIa and kallikrein processed pro-HGF by cleavage at two sites. Using N-terminal sequencing they were identified as the normal cleavage site Arg(494)-Val(495) and the novel site Arg(424)-His(425) located in the K4 domain of the alpha-chain. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256512 |
Arg494 |
CAKTKQLrVVNGIPT |
in vitro |
|
| pmid |
sentence |
| 12372819 |
the ability of plasma kallikrein and FXIa to activate pro-HGF in vitro raises the possibility that mediators of inflammation and blood coagulation may also regulate processes that involve the HGF/c-Met pathway, such as tissue repair and angiogenesis.Unlike other known activators, both FXIa and kallikrein processed pro-HGF by cleavage at two sites. Using N-terminal sequencing they were identified as the normal cleavage site Arg(494)-Val(495) and the novel site Arg(424)-His(425) located in the K4 domain of the alpha-chain. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
SP3 | up-regulates quantity by expression
transcriptional regulation
|
HGF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251741 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 9223667 |
Furthermore, in transient cotransfection assays, overexpression of Sp1 and/or Sp3 stimulated HGF promoter activity independently and additively through binding to the Sp1 binding site in the HGF gene promoter region. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SP1 | up-regulates quantity by expression
transcriptional regulation
|
HGF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251739 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 9223667 |
Furthermore, in transient cotransfection assays, overexpression of Sp1 and/or Sp3 stimulated HGF promoter activity independently and additively through binding to the Sp1 binding site in the HGF gene promoter region. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
HGF | up-regulates
binding
|
MET |
0.927 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-38429 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8380735 |
Hgf is the ligand for p190met, the receptor tyrosine kinase encoded by the met proto-oncogene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor, Prostate Cancer, Rhabdomyosarcoma |
| + |
TWIST1 | up-regulates quantity by expression 
transcriptional regulation
|
HGF |
0.332 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255522 |
|
|
Homo sapiens |
GBM-8401 Cell |
| pmid |
sentence |
| 20646316 |
Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT3 | up-regulates quantity by expression
transcriptional regulation
|
HGF |
0.608 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251742 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11278729 |
Coexpression of activated c-Src and Stat3 synergistically induced strong HGF promoter activity in SP1 cells |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Rhabdomyosarcoma |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263657 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25122198 |
we identified pro-hepatocyte growth factor (HGF) as a TMPRSS2 substrate and confirmed that HGF and it’s cognate receptor c-Met are activated in prostate cancers expressing TMPRSS2, a finding that also associated with the acquisition of a pro-invasive mesenchymal gene expression program. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Prostate Cancer |
3.0
HGF
- 
- 